Characterization of spontaneous, transient adenosine release in the caudate-putamen and prefrontal cortex

Adenosine is a neuroprotective agent that inhibits neuronal activity and modulates neurotransmission. Previous research has shown adenosine gradually accumulates during pathologies such as stroke and regulates neurotransmission on the minute-to-hour time scale. Our lab developed a method using carbo...

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Published in:	PloS one 2014-01, Vol.9 (1), p.e87165-e87165
Main Authors:	Nguyen, Michael D, Lee, Scott T, Ross, Ashley E, Ryals, Matthew, Choudhry, Vishesh I, Venton, B Jill
Format:	Article
Language:	eng
Subjects:	Adenosine Adenosine - secretion Adenosine A1 Receptor Agonists - pharmacology Adenosine A1 Receptor Antagonists - pharmacology Animals Biology Biosensors Carbon Caudate-putamen Change detection Chemistry Dopamine Electrodes Hypoxia Implantation In vivo methods and tests Ischemia Laboratory animals Male Metabolites Microelectrodes Nervous system Neuromodulation Neurons Neuroprotection Neurosciences Neurotransmission Prefrontal cortex Prefrontal Cortex - drug effects Prefrontal Cortex - metabolism Putamen Putamen - drug effects Putamen - metabolism Rats Receptor, Adenosine A1 - metabolism Receptors Rodents Signaling Spinal cord Surgical implants Time Voltammetry
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Summary:	Adenosine is a neuroprotective agent that inhibits neuronal activity and modulates neurotransmission. Previous research has shown adenosine gradually accumulates during pathologies such as stroke and regulates neurotransmission on the minute-to-hour time scale. Our lab developed a method using carbon-fiber microelectrodes to directly measure adenosine changes on a sub-second time scale with fast-scan cyclic voltammetry (FSCV). Recently, adenosine release lasting a couple of seconds has been found in murine spinal cord slices. In this study, we characterized spontaneous, transient adenosine release in vivo, in the caudate-putamen and prefrontal cortex of anesthetized rats. The average concentration of adenosine release was 0.17±0.01 µM in the caudate and 0.19±0.01 µM in the prefrontal cortex, although the range was large, from 0.04 to 3.2 µM. The average duration of spontaneous adenosine release was 2.9±0.1 seconds and 2.8±0.1 seconds in the caudate and prefrontal cortex, respectively. The concentration and number of transients detected do not change over a four hour period, suggesting spontaneous events are not caused by electrode implantation. The frequency of adenosine transients was higher in the prefrontal cortex than the caudate-putamen and was modulated by A1 receptors. The A1 antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine, 6 mg/kg i.p.) increased the frequency of spontaneous adenosine release, while the A1 agonist CPA (N(6)-cyclopentyladenosine, 1 mg/kg i.p.) decreased the frequency. These findings are a paradigm shift for understanding the time course of adenosine signaling, demonstrating that there is a rapid mode of adenosine signaling that could cause transient, local neuromodulation.
ISSN:	1932-6203 1932-6203